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JKC MOD- Spring '24 > Lecture 2- Acute Inflammation/Shock > Flashcards

Lecture 2- Acute Inflammation/Shock Flashcards

1
Q

Name some examples of first line of defense

A

Skin, tears, saliva, gut flora, gastric acid

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2
Q

What is the second line of defense?

A

Inflammatory response

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3
Q

What is the third line of defense?

A

Immune response

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4
Q

The immune response is very specific or non-specific?

A

nonspecific

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5
Q

Name some causes of acute inflammation.

A

Microorganisms
Hypoxia/Ischemia
Nutritional deficiencies
Trauma/Surgery
Radiation
Caustic chemicals
Extreme heat/cold (Sunburn and frost bite)

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6
Q

What are the 2 major components of acute inflammation?

A

Vascular and Cellular response

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7
Q

Describe what happens during the vascular response portion of acute inflammation.

A

Initially the vessels will constrict, then dilate and being more permeable.

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8
Q

Why do the vessels constrict as the first reaction?

A

Because they want to prevent blood loss

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9
Q

What 2 things does vasodilation lead to

A
  1. Increased blood flow to the area
  2. Enhances transport of blood and cells
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10
Q

Name the 3 major patterns of vascular response

A
  1. Immediate Transient- Minor injury
  2. Immediate sustained- major injury
  3. Delayed hemodynamic- 4-24 hours after injury
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11
Q

What are the 4 steps of the cellular response to acute inflammation.

A
  1. Margination/adhesion
  2. Migration (Diapedesis)
  3. Chemotaxis
  4. Phagocytosis
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12
Q

_____ are released when cells are injured

A

Cytokines

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13
Q

Cytokines influence endothelial cells to produce _____

A

Selectins

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14
Q

In Professor Jensen’s analogy, what molecules are the velcro strips?

A

Selectins

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15
Q

Describe what happens during the margination phase of cellular response.

A

Injury causes cytokines to be released, cytokines influence the cell to release selectins, leukocytes slow migration due to the selectins and begin adhering to the vessel wall

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16
Q

Leukocytes naturally will travel towards….

A

the area where they are in the highest concentration (chemotaxis) aka the site of the injury

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17
Q

Following chemotaxis, the leukocytes being ______.

A

phagocytosis

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18
Q

Define opsonization

A

Where the harmful “bacteria” or whatever is the source gets tagged for destruction/engulfment

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19
Q

Leukocytes can only crawl out of
A. Arteries
B. Veins/Capillaries
C. Both. arteries and veins

A

Veins only

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20
Q

Why can leukocytes only move out of veins?

A

Because arteries have lots of smooth muscle surrounding the vessel vs veins have very little smooth muscle surrounding the vessel

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21
Q

Neutrophils (PMNs or Segs) are the _______ to respond to an injury site. How long does it take to arrive?

A

First, 90 minutes and survive

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22
Q

Define leukocytosis

A

Increased WBC in the blood

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23
Q

Define banding

A

Where immature forms of neutrophils are released early due to an increased demand

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24
Q

Define left shift

A

Where immature forms of neutrophils are released early due to an increased demand

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25
Q

What kind of cell is this?

A

Lymphocyte

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26
Q

What kind of cell is this?

A

PMN

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27
Q

What kind of cell is this?

A

Band

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28
Q

What kind of cell is this?

A

Platelet

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29
Q

What kind of cell is this?

A

PMNs

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30
Q

What kind of cell is this?

A

Monocyte

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31
Q

What kind of cell increased with allergic reactions and parasitic infections?

A

Eosinophils

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32
Q

Granulocytes differentiate into 4 different types. Name them.

A

Mast cell
Basophil
Eosinophil
Neutrophil

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33
Q

______ increase with inflammation and allergic reaction

A

Basophils

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34
Q

______ release histamine and bond with IgE

A

Basophils

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35
Q

______ are similiar to basophils but in connective tissue

A

Mast cells

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36
Q

______ sit at the entrance and sound the alarm whenever they see something they perceive as a threat. “Sentinel position”

A

Mast cells

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37
Q

What kind of cell?

A

Mast cell

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38
Q

What kind of cell?

A

Basophil

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39
Q

What kind of cell?

A

Eosinophil

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40
Q

What kind of cell?

A

Neutrophil

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41
Q

_______ are not granulocytes

A

Monocytes

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42
Q

Monocytes are the ______ WBC

A

Largest

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43
Q

When do monocytes typically arrive to the injury?

A

approximately 24 hours after the injury

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44
Q

______ are the predominant cell type approx 48 hours after the injury

A

Monocyte

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45
Q

Why are monocytes the better choice in the long run?

A

More efficient, larger so they can engulf more pathogens, recognize certain types of pathogens to signal other specific help

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46
Q

_______ transport oxygen to tissues

A

Erythrocytes

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47
Q

________ help mediate a vascular response

A

Thrombocytes

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48
Q

_______ release inflammatory mediators

A

Thrombocytes

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49
Q

________ synthesize and release inflammatory mediators

A

Endothelial cells

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50
Q

_______ release selectins

A

Endothelial cells

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51
Q

_______ is the most important kinin in inflammatory response

A

Bradykinin

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52
Q

Name 3 properties of kinins:

A
  1. Vasodilation and increased vascular permeability
  2. Smooth muscle contraction (gut, lungs, etc, trying to kick out pathogens)
  3. involved with the pain response
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53
Q

_______ is broken down by kininase and angiotensin-converting enzyme

A

Bradykinin

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54
Q

_______ is formed during the clotting process

A

Fibrinopeptides

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55
Q

_______ key protease enzyme in the clotting process

A

Thrombin

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56
Q

Name 2 important functions of the clotting system in the inflammatory response

A
  1. Expression of endothelial adhesion molecules
  2. Production of prostaglandins, PAF and chemokines
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57
Q

Name 5 major functions of complement in the inflammatory response.

A
  1. Vasodilation and increased vascular permeability
  2. Smooth muscle contraction
  3. Leukocyte activation, adhesion and chemotaxis
  4. Augmentation of phagocytosis
  5. Mast cell degranulation
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58
Q

_____ and ______ complement is important for inflammation

A

C3a and C5a

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59
Q

Histamine is released from what 3 types of cells

A

Mast cells
Basophils
Platelets

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60
Q

______ is one of the first mediators of inflammation

A

Histamine

61
Q

______ plays a major role in the vascular inflammatory response via _____ receptor

A

Histamine, H1

62
Q

When vasodilation happens does vascular permeability increase or decrease?

A

Increase

63
Q

_____ includes chemokines, interferons (IFNs), interleukins(ILs), lymphokines, and tumor necrosis factor (TNF)

A

Cytokines

64
Q

Name 3 Cytokine specifice examples mediators of early inflammatory response.

A

IL-1
IL-6
TNF-α

65
Q

The cytokine major mediators of early inflammatory response result in what 5 things.

A

Fever
Adhesion of leukocytes to vessel epithelium
Chemotaxis
General acute-phase response
Also involved in pain response

66
Q

______, ______ and _______ are derived from Arachidonic acid

A

Prostaglandins, leukotrienes and Thromboxane

67
Q

________ is a fatty acid precursor derived from phospholipids in cell membrane

A

Arachidonic acid

68
Q

Cyclooxygenase pathway leads to ______

A

Prostaglandins

69
Q

The Lipoxygenase pathway leads to _____

A

Leukotrienes

70
Q

________ induce smooth muscle contraction, constricts pulmonary airways, increases microvascular permeability

A

Leukotrienes

71
Q

Give some examples of Leukotrienes

A
72
Q

_______ induces vasodilation and bronchoconstriction, inhibits inflammatory cell function

A

Prostaglandins

73
Q

Give some examples of Prostaglandins

A
74
Q

_______ vasoconstriction, Bronchoconstriction, promotes platelet function

A

Thromboxane

75
Q

Give an example of Thromboxane

A

TxA2

76
Q

______ promote vascular permeability and vasodilation. Involved in the pain response

A

Prostaglandins

77
Q

______ and ______ induce inflammation and potentiate effects of other inflammatory mediators, especially histamine

A

Prostaglandin E1 (PGE1) and Prostaglandin E2 (PGE2)

78
Q

______ promotes platelet aggregation and vasoconstriction

A

Thromboxane A2

79
Q

_____ and ______ inhibit enzyme in cyclooxygenase pathway for prostaglandin synthesis

A

NSAIDs and Aspirin

80
Q

_______ are similar to histamine but are not readily available. They have to be made versus histamine is kept on hand

A

Leukotrienes

81
Q

Name some functions of Leukotrienes

A

Vascular permeability, endothelial adhesion, chemotaxis, more histamine release

82
Q

What are Slow-Reacting Substance of Anaphylaxis (SRS-A)

A

a group of leukotrienes that cause slow and sustained constriction of bronchioles. Important factor in asthmatic bronchitis, anaphylaxis

83
Q

______ are used in treatment of asthma

A

Leukotriene receptor antagonists

84
Q

______ block enzyme in lipoxygenase pathway to convert arachidonic acid to leukotrienes

A

5-lipoxygenase inhibitors

85
Q

_______ are derived from cell membrane phospholipids

A

Platelet Activating Factor (PAF)

86
Q

Name some functions of Platelet Activating Factor (PAF)

A

Activates platelets by Induces platelet aggregation
Increased vascular permeability
Neutrophil activation
Chemoattractant for eosinophils

87
Q

_______ stimulates platelets to release vasoactive
mediators and synthesize thromboxanes

A

Platelet Activating Factor (PAF)

88
Q

_______ is an inflammatory mediators

A

Nitric oxide

89
Q

Name some functions of Nitric Oxide

A

-Smooth muscle relaxation
-Antagonism of platelet functions
(Adhesion, aggregation, degranulation)
-Reduces leukocyte recruitment
-Assists in microbicidal action
by phagocytes

90
Q

What causes Erythema?

A

Vasodilation, increased blood flow

91
Q

What causes heat?

A

Vasodilation, increased blood flow

92
Q

What causes swelling?

A

Increased vascular permeability and increased fluid in extracellular space

93
Q

What causes pain?

A

Compression of tissues due to swelling, direct elicitation of pain due to inflammatory mediators

94
Q

What causes loss of function?

A

Direct damage to tissue from injury, decreased function due to pain and swelling

95
Q

Define exudate

A

Fluid excreted from site of injury due to vascular response

96
Q

Define serous

A

watery, lower in protein; derived from plasma entering inflammatory site

97
Q

Define sanguinous

A

thin, red or pink, watery; plasma with a few RBCs mixed in

98
Q

______ large amounts of fibrinogen - thick, sticky meshwork (adhesions)

A

Fibrinous

99
Q

Define purulent

A

Pus

100
Q

______ severe tissue injury causing damage to blood vessels or significant leakage of RBCs from capillaries (hematoma)

A

Hemorrhagic

101
Q

______ form on mucous membranes; necrotic cells in fibropurulent base

A

Membranous/Pseudomembranous

102
Q

______ localized area of inflammation containing purulent exudate. Often walled off from healthy tissue by fibroblasts

A

Abscess

103
Q

_____ necrotic, eroded area of epithelium with subepithelial inflammation. Can be due to traumatic injury or vascular compromise

A

Ulceration

104
Q

Acute-Phase response often includes:

A

Fever, Increased numbers of leukocytes, lethargy, skeletal muscle catabolism, increased Erythrocyte Sedimentation Rate (ESR)

105
Q

In the acute-phase response a fever is cause by what specific factors

A
  • cause by IL-1, IL-6, TNF-α
  • Resetting of thermoregulatory set point in hypothalamus
106
Q

Acute-phase reaction causes liver to dramatically increase production of proteins like ______ and ______ that play a role in the immune response

A

Fibrinogen and C-reactive protein (CRP)

107
Q

_____ binds to surface of invading microorganisms to assist their destruction

A

CRP

108
Q

Elevated CRP indicate…..

A

Large inflammatory response is active.

Infection, sleep deprivation (mild elevation), HTN, DM, smoking, aging, obesity and depression

109
Q

CRP can be used to look for risk of other diseases such as…

A

inflammatory and autoimmune disease

110
Q

Elevated CRP is associated with increased ____ ______ risk

A

Cardiovascular disease

111
Q

Sed rate is define as

A

how quickly RBC clump together. faster they clump the more inflammation

112
Q

Why is sed rate falsely elevated in anemic patients?

A

Because they have less RBC overall with so the clumping is faster due to less volume

113
Q

______ changes more slowly in response to inflammation activity than CRP

A

Sed Rate (ESR)

114
Q

_______ increase in overall number of WBCs in the serum

A

Leukocytosis

115
Q

_______ cause WBC to go up

A

Steroids

116
Q

Certain medication and bone marrow disease can cause…..

A

Elevated WBC

117
Q

In a CBC w/diff, the neutrophils are elevated, what type of reaction does this indicate?

A

Bacterial infection

118
Q

In a CBC w/diff, the eosinophils are elevated, what type of reaction does this indicate?

A

Parasitic infection or allergic reaction

119
Q

In a CBC w/diff, the neutrophils and/or lymphocytosis are elevated, what type of reaction does this indicate?

A

viral infection

120
Q

In a CBC w/diff, a left shift is elevated, what type of reaction does this indicate?

A

Infection

121
Q

______ inflammatory reaction in lymph NODES draining an injured area caused by filtering lymph fluid with infection material draining from local injured or infected areas

A

Lymphadenitis

122
Q

How do you treat lymphadenitits?

A

Solve whatever is causing the inflammation, using through antimicrobial therapy, analgesics, anti-inflammatories, cool compresses.

Abscessed nodes may require drainage

123
Q

Inflammation or infection of lymph VESSEL draining an injured area

A

Lymphangitis

124
Q

Red, tender streaks extending proximally is a sign of _______

A

Lymphangitis

125
Q

Streptococcus pyogenes also coincides with _____

A

Lymphangitis

126
Q

Define shock

A

Life-threatening condition caused by lack of adequate circulation and oxygenation of the body

127
Q

What are some signs of shock:

A

-Extremely low blood pressure (hypotension)
-Decreased urine output (oliguria)
-Pale, cool, clammy skin
-Altered mental status
Early - agitation, irritability, and/or anxiety
Late - confusion, delirium, coma
-Metabolic acidosis

128
Q

Name some other signs of shock

A

-Shallow breathing and/or rapid breathing (tachypnea)
-Elevated heart rate (tachycardia)
-Dehydration
-Chest pain and/or irregular heartbeat

129
Q

Name the 5 kinds of shock

A
  1. Cardiogenic Shock
  2. Hypovolemic Shock
  3. Anaphylactic Shock
  4. Neurogenic Shock
  5. Septic Shock
130
Q

_____ severe, rapid allergic or hypersensitivity reaction with potential to be fatal

A

Anaphylactic Shock

131
Q

_______ : damage to the autonomic CNS pathways
Sudden loss of sympathetic stimulation to blood vessels → massive vasodilation → sudden hypotension

A

Neurogenic Shock

132
Q

_______: systemic vasodilation secondary to infection and dysregulation of inflammatory response

A

Septic Shock

133
Q

_______ : due to inability of heart to pump the required amount of blood

A

Cardiogenic Shock

134
Q

Name some causes of Cardiogenic shock

A

cardiac arrhythmias, damaged heart muscle or valves, pressure around heart inhibiting cardiac movement, rupture of heart muscle

135
Q

______: decreased intravascular volume leading to decreased perfusion of vital organs

A

Hypovolemic Shock

136
Q

Name 2 causes of Hypovolemic Shock

A

caused by hemorrhage or fluid loss

137
Q

Broad category of shock due to severe vasodilation causing loss of peripheral vascular resistance

A

Distributive Shock

138
Q

Distributive shock inclues what 3 types:

A
  1. anaphylactic shock
  2. neurogenic shock
  3. septic shock
139
Q

______ Exaggerated, unregulated, self-sustaining inflammatory response to an infection

A

Septic shock

140
Q

______ systemic uncontrolled inflammatory response

A

Septic shock

141
Q

Septic shock is largely mediated by ____ and _____.

A

IL-1 and TNF-α

142
Q

Septic shock leads to what 4 things.

A
  1. excessive vasodilation
  2. tissue ischemia
  3. direct cell injury
  4. altered rate of apoptosis
143
Q

During what kind of shock do multiple organ systems suffer severe negative impacts

A

Septic shock

144
Q

Septic shock circulatory, what happens?

A

severe hypotension and hypoperfusion

Excessive vasoactive mediators → decreased vascular resistance
Third spacing of fluid → increased vascular permeability

145
Q

Septic shock lungs, what happens?

A

pulmonary edema and hypoxemia

146
Q

Septic shock kidney, what happens?

A

-Impaired filtration of toxins and waste products
-Hypoperfusion
-Direct renal damage

147
Q

Septic shock GI tract, what happens?

A

increased intestinal permeability allowing bacteria and bacterial endotoxins in gut to enter systemic circulation

148
Q

Septic shock Liver, what happens?

A

-Impaired elimination of bacteria and endotoxins from gut
-Hypoperfusion
-Direct cellular injury

149
Q

Septic shock nervous system, what happens?

A

Encephalopathy due to changes in cell signaling caused by inflammatory mediators; dysfunction of blood-brain barrier

JKC MOD- Spring '24 (10 decks)

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